Impairment in social cognition- the mental abilities involved in adaptive interpersonal interactions-is increasingly being recognized as a key feature of schizophrenia (SZ). Social cognitive impairment in SZ is pervasive and contributes significantly to poor functioning and overall quality of life. However, despite a growing body of literature, there is no overarching framework to satisfactorily explain the impairment seen in SZ across multiple social cognitive domains (e.g., facial affect recognition, mental state attribution. Identifying such a framework would substantially improve our understanding of the disease and could be valuable for the development of novel interventions to improve social cognition in SZ. With this as the long-term research goal, this exploratory R21 project focuses on a core feature of social information processing, the social preference system (SPS), and will evaluate whether a disrupted SPS is a plausible underlying factor for social cognitive impairment in SZ. The prioritized processing of social information is referred to as the social preference system (SPS). Examples of the SPS include: preferential orienting to social over nonsocial information (i.e., social orienting) and seeking and enjoying social over nonsocial information (i.e., social reward). When processing social information is prioritized, the opportunity to perceive and experience social stimuli and to respond appropriately increases, thereby developing social cognitive skills. Consistent with this view, emerging evidence from basic science strongly supports the critical role of the SPS in the development of social cognition. Further, unique neural areas associated with the SPS have recently been identified. Overall a disrupted SPS is a plausible explanation of social cognitive impairment in SZ. To empirically examine this possibility, we hypothesize that SZ patients have a disrupted SPS and that the downstream effect of this disruption is impaired social cognition, while nonsocial cognition is not affected by the disrupted SPS. With 35 SZ patients and 35 healthy controls over 2 years, we will employ a multi-modal approach (i.e., performance, neuroimaging and self-report questionnaires) with a focus on social orienting and social reward, and will evaluate the following scientific aims: 1) To examine whether SZ patients show a disrupted SPS and whether the downstream effect of the SPS is present in social cognition but not in nonsocial cognition; and 2) To examine whether SZ patients show aberrant neural activations related to the SPS. The findings of this project could be valuable for determining the underlying causes of social cognitive impairment in SZ and could provide insights into our understanding of social cognitive impairment in other psychiatric illnesses. In this regard, this project is consistent with the NIMH Strategic Plan I Objective 1: Promote Discovery in the Brain and Behavioral Science to Fuel Research on the Causes of Mental Disorders and with the NIMH Research Domain Criteria (RDoC) Project.